Evidence map›Paper›PMID 33052479›Full record

ReviewInflammopharmacology2021

Neuroinflammatory responses in Parkinson's disease: relevance of Ibuprofen in therapeutics.

Ashish Singh, Pratibha Tripathi, Sarika Singh

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Related Mechanism of Limonene Improves LPS-Induced Neuroinflammation.Journal of microbiology and biotechnology · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Observational
  10. Review
  11. Article
  12. Review
  13. Investigation of the peripheral inflammation (neutrophil-lymphocyte ratio) in two neurodegenerative diseases of the central nervous system.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ashish SinghDepartment of Neuroscience and Ageing Biology, Division of Toxicology and Experimental Medicine, Central Drug Research Institute, Lucknow, Uttar Pradesh, 226031, India.
Pratibha TripathiDivision of Pharmacology, Central Drug Research Institute, Lucknow, Uttar Pradesh, 226031, India.
Sarika SinghDepartment of Neuroscience and Ageing Biology, Division of Toxicology and Experimental Medicine, Central Drug Research Institute, Lucknow, Uttar Pradesh, 226031, India. sarika_singh@cdri.res.in.ORCID http://orcid.org/0000-0001-6195-9029
Central Drug Research Institute · IN

Funding

Indian Council of Medical Research 2016-0624/CMB/Adhoc-BMSScience and Engineering Research Board PDF/2017/000984
6 · The paper itself

Abstract

Parkinson's disease (PD) pathogenesis inevitably involves neuroinflammatory responses attained through contribution of both neuron and glial cells. Investigation done in both experimental models of PD and in samples of PD patients suggested the involvement of both central and peripheral inflammatory responses during PD pathogenesis. Such neuroinflammatory responses could be regulated by neuron-glia interaction which is one of the recently focused areas in the field of disease diagnosis, pathogenesis and therapeutics. Such aggravated neuroinflammatory responses during PD are very well associated with augmented levels of cyclooxygenase (COX). An increased expression of cyclooxygenase (COX) with a concomitant increase in the prostaglandin E2 (PGE2) levels has been observed during PD pathology. Ibuprofen is one of the non-steroidal anti-inflammatory drugs (NSAID) and clinically being used for PD patients. This review focuses on the neuroinflammatory responses during PD pathology as well as the effect of ibuprofen on various disease related signaling factors and mechanisms involving nitrosative stress, neurotransmission, neuronal communication and peroxisome proliferator-activated receptor-γ. Such mechanistic effect of ibuprofen has been mostly reported in experimental models of PD and clinical investigations are still required. Since oxidative neuronal death is one of the major neurodegenerative mechanisms in PD, the antioxidant capacity of ibuprofen along with its antidepressant effects have also been discussed. This review will direct the readers towards fulfilling the existing gaps in the mechanistic aspect of ibuprofen and enhance its clinical relevance in PD therapeutics and probably in other age-related neurodegenerative diseases.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalAntioxidantsHumansIbuprofenInflammationNeurogliaNeuronsParkinson DiseaseParkinsonian DisordersProstaglandin-Endoperoxide SynthasesAnti-Inflammatory Agents, Non-SteroidalAntioxidantsIbuprofenProstaglandin-Endoperoxide SynthasesCOXDiseaseNeuroprotectionNon-steroidal anti-inflammatory drugParkinsons

Identifiers

PMID33052479
OpenAlexW3092419615

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.